Longevity and Gross Pathology At Death in 22 Inbred Mouse Strains

Storer, John B.

doi:10.1093/geronj/21.3.404

Cited by 209 publications

(82 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Each mouse was monitored daily by the research team and vivarium staff from 6 weeks of age to the end of the lifespan. Maximal lifespan of a male CBA/J mouse has been noted to be approximately 75 to 85 weeks of life (Storer 1966;Tillmann et al 2000). At 93 weeks of age, all mice were anesthetized with isoflurane gas at 4.0 % concentration in oxygen with a 800 cm 3 /min flow rate.…”

Section: Animal Subjectsmentioning

confidence: 99%

Altered left ventricular performance in aging physically active mice with an ankle sprain injury

Turner

Guderian

Wikstrom

et al. 2016

AGE

View full text Add to dashboard Cite

We assessed the impact of differing physical activity levels throughout the lifespan, using a musculoskeletal injury model, on the age-related changes in left ventricular (LV) parameters in active mice. Forty male mice (CBA/J) were randomly placed into one of three running wheel groups (transected CFL group, transected ATFL/CFL group, SHAM group) or a SHAM Sedentary group (SHAMSED). Before surgery and every 6 weeks after surgery, LV parameters were measured under 2.5 % isoflurane inhalation. Group effects for daily distance run was significantly greater for the SHAM and lesser for the ATLF/CFL mice (p = 0.013) with distance run decreasing with age for all mice (p < 0.0001). Beginning at 6 months of age, interaction (group × age) was noted with LV posterior wall thickness-to-radius ratios (h/r) where h/r increased with age in the ATFL/CFL and SHAMSED mice while the SHAM and CFL mice exhibited decreased h/r with age (p = 0.0002). Passive filling velocity (E wave) was significantly greater in the SHAM mice and lowest for the ATFL/CFL and SHAMSED mice (p < 0.0001) beginning at 9 months of age. Active filling velocity (A wave) was not different between groups (p = 0.10). Passive-to-active filling velocity ratio (E/A ratio) was different between groups (p < 0.0001), with higher ratios for the SHAM mice and lower ratios for the ATFL/CFL and SHAMSED mice in response to physical activity beginning at 9 months of age. Passive-toactive filling velocity ratio decreased with age (p < 0.0001). Regular physical activity throughout the lifespan improved LV structure, passive filling velocity, and E/A ratio by 6 to 9 months of age and attenuated any negative alterations throughout the second half of life. The diastolic filling differences were found to be significantly related to the amount of activity performed by 9 months and at the end of the lifespan.

show abstract

Section: Animal Subjectsmentioning

confidence: 99%

Altered left ventricular performance in aging physically active mice with an ankle sprain injury

Turner

Guderian

Wikstrom

et al. 2016

AGE

View full text Add to dashboard Cite

show abstract

“…136,194,209 Several references from the past century offer potentially useful perspectives on the history and expected phenotypes of inbred mice. 132,140,163,166,202 Some additional references are especially relevant to understanding the spectrum of pathology in mice of various strains or stocks. 39,40,41,73,146,159,175 Tables 3 and 4 summarize common pathology findings from large and long-term (>1 year) studies involving 16 inbred strain families and several non-inbred stocks.…”

Section: Genetic Background: Expected Pathology Phenotypes and Causesmentioning

confidence: 99%

Pathobiology of Aging Mice and GEM

2012

View full text Add to dashboard Cite

The use of induced and spontaneous mutant mice and genetically engineered mice (and combinations thereof) to study cancers and other aging phenotypes to advance improved functional human life spans will involve studies of aging mice. Genetic background contributes to pathology phenotypes and to causes of death as well as to longevity. Increased recognition of expected phenotypes, experimental variables that influence phenotypes and research outcomes, and experimental design options and rationales can maximize the utility of genetically engineered mice (GEM) models to translational research on aging. This review aims to provide resources to enhance the design and practice of chronic and longevity studies involving GEM. C57BL6, 129, and FVB/N strains are emphasized because of their widespread use in the generation of knockout, transgenic, and conditional mutant GEM. Resources are included also for pathology of other inbred strain families, including A, AKR, BALB/c, C3H, C57L, C58, CBA, DBA, GR, NOD.scid, SAMP, and SJL/J, and non-inbred mice, including 4WC, AB6F1, Ames dwarf, B6, 129, B6C3F1, BALB/c,129, Het3, nude, SENCAR, and several Swiss stocks. Experimental strategies for long-term cross-sectional and longitudinal studies to assess causes of or contributors to death, disease burden, spectrum of pathology phenotypes, longevity, and functional healthy life spans (health spans) are compared and discussed.

show abstract

“…While the 129S2/SvHsd substrain also has a low incidence of spontaneous tumors, its level of radiosensitivity leading to early-onset tumors, including rAML, has been unknown (28). Our in vivo experiments demonstrated similar mean life spans for 129S2/SvHsd and CBA/H after 3 Gy X irradiation, when normalized to controls (82% and 75%, respectively) (Supplementary Table S2, http://dx.doi.org/10.…”

Section: Discussionmentioning

confidence: 59%